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Alanine–serine–cysteine transporter 2 (ASCT2, SLC1A5) is a plasma membrane sodium-dependent transporter responsible primarily for **glutamine import** in human cells[1][3]. Despite its historical name indicating specificity for alanine, serine, and cysteine, its major functional role is as a high-affinity glutamine transporter, with cysteine acting as a modulator rather than a substrate[1]. ASCT2 operates as an obligate exchanger, mediating the bidirectional transport of neutral amino acids but is especially important for **glutamine influx** in rapidly proliferating cells, notably in many cancers where its expression is upregulated and correlates with poor prognosis[2][3][4]. ASCT2 is also involved in the regulation of intracellular amino acid homeostasis, and its inhibition represents a promising strategy for anticancer therapy by depriving tumor cells of glutamine, an essential metabolic resource for growth and survival. Beyond cancer, its normal physiological activity supports demanding tissues and immune responses. ASCT2 is regulated by post-translational modifications and interactions with other cellular proteins. It has also been exploited by certain retroviruses as a cellular entry receptor[1].
Inhibition of glutamine transport (blocks cellular glutamine uptake, starves glutamine-dependent tumor cells[2][4]) Modulation of neutral amino acid exchange
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